The 17 shortlisted studies targeted GSK3β (via SAR502250 [132]; tideglusib [130]; lithium chloride [133, 179, 180]; AR-A014418 [133]; MMBO [135]); CDK-5 (via ®-roscovitine [136]), p38MAPK (via MW181; SB239063 [137]); c-Abl and Src (via nilotinib [138]; bosutinib [138]), Fyn (AZD0530 [181]), DYRK1A (via Dryk1-inh [140]; DYR219 [141]; SM07883 [139]), MARK4 (dl-NBP [182]), SYK (BAY61 [142]) and Rho-kinase (Fasudil) [143] inhibition, which resulted in cumulative reduction of tau hyperphosphorylation and alleviation of the AD cognitive/behavioural phenotype. This evidence concerns the gene MARK4 and Alzheimer disease.